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NeurosciencesMultimodal Imaging and Prediction of Cognitive Dysfunction |
1 Nuclear Medicine, Technische Universität München, Munich, Germany 2 Psychiatry, Technische Universität München, Munich, Germany
Abstract No. 305
Objectives: Anatomical overlap between amyloid-pathology and local synaptic dysfunction, reflected in hypometabolism has been shown in patients with Alzheimers disease (AD). In some brain areas distinct hypometabolism despite only minor amyloid-pathology is found (hypometabolism only = HO), which cannot easily be explained by local neurotoxicity. Aim of this multimodal imaging study was to explore if HO may be a consequence of amyloid-pathology in functionally connected, remote brain regions.
Methods: 19 AD-patients and 15 elderly controls attended an examination with [11C]PIB-PET and [18F]FDG-PET. Group comparisons between patients and controls were performed and HO was detected by subtracting of equally thresholded result-maps (SPM5, p<0.01 FDR-corr). In a second step, HO was used as a seed for a functional connectivity analysis in resting state fMRI data of 17 healthy controls. This network of HO-connected areas (CAs) was retransferred into the brains of AD-patients to analyze pathologies in the PET-datasets. Quantitative relations between FDG-SUVR in HO, in CAs and in brain-areas outside CAs were substantiated by correlation analyses.
Results: In the AD-group, a prominent HO-area was detected in the left superior frontal gyrus. CAs of this seed in healthy controls were preferably located in parietal areas. Retransferred in the brains of AD-patients, the CAs were predominantly located in areas affected by amyloid-pathology and hypometabolism. This association could be quantified by a strong correlation between FDG-SUVR in HO and CAs (r=0.912), significantly stronger than between HO and areas outside CAs (r=0.697, p=0.027).
Conclusions: A strong correlation between metabolism in HO-areas and in amyloid-affected CAs has been demonstrated in AD. These results support the assumption that hypometabolism in brain regions not strongly affected by amyloid-pathology may be caused by diminished neuronal input from affected regions
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